Subacute Pain after Traumatic Brain Injury Is Associated with Lower Insular N

Persistent pain is experienced by more than 50% of persons who sustain a traumatic brain injury (TBI), and more than 30% experience significant pain as early as 6 weeks after injury. Although neuropathic pain is a common consequence after CNS injuries, little attention has been given to neuropathic pain symptoms after TBI. Magnetic resonance spectroscopy (MRS) studies in subjects with TBI show decreased brain concentrations of N-acetylaspartate (NAA), a marker of neuronal density and viability. Although decreased brain NAA has been associated with neuropathic pain associated with spinal cord injury (SCI) and diabetes, this relationship has not been examined after TBI. The primary purpose of this study was to test the hypothesis that lower NAA concentrations in brain areas involved in pain perception and modulation would be associated with greater severity of neuropathic pain symptoms. Participants with TBI underwent volumetric MRS, pain and psychosocial interviews. Cluster analysis of the Neuropathic Pain Symptom Inventory subscores resulted in two TBI subgroups: The Moderate Neuropathic Pain (n = 17; 37.8%), with significantly (p = 0.038) lower insular NAA than the Low or no Neuropathic Pain group (n = 28; 62.2%), or age- and sex-matched controls (n = 45; p < 0.001). A hierarchical linear regression analysis controlling for age, sex, and time post-TBI showed that pain severity was significantly (F = 11.0; p < 0.001) predicted by a combination of lower insular NAA/Creatine (p < 0.001), lower right insular gray matter fractional volume (p < 0.001), female sex (p = 0.005), and older age (p = 0.039). These findings suggest that neuronal dysfunction in brain areas involved in pain processing is associated with pain after TBI

Data sonification for Bachelor of Computer science in US from 1966 to 1999.

Recent years have seen a rejuvenation of interest in studies of motivation-cognition interactions arising from many different areas of psychology and neuroscience. The present issue of Cognitive, Affective, & Behavioral Neuroscience provides a sampling of some of the latest research from a number of these different areas. In this introductory article, we provide an overview of the current state of the field, in terms of key research developments and candidate neural mechanisms receiving focused investigation as potential sources of motivation-cognition interaction. However, our primary goal is conceptual: to highlight the distinct perspectives taken by different research areas, in terms of how motivation is defined, the relevant dimensions and dissociations that are emphasized, and the theoretical questions being targeted. Together, these distinctions present both challenges and opportunities for efforts aiming toward a more unified and cross-disciplinary approach. We identify a set of pressing research questions calling for this sort of cross-disciplinary approach, with the explicit goal of encouraging integrative and collaborative investigations directed toward them

Cloning, characterization, and tissue distribution of prolactin receptor in the sea bream (Sparus aurata)

The prolactin receptor (PRLR) was cloned and its tissue distribution characterized in adults of the protandrous hermaphrodite marine teleost, the sea bream (Sparus aurata). An homologous cDNA probe for sea bream PRLR (sbPRLR) was obtained by RT-PCR using gill mRNA. This probe was used to screen intestine and kidney cDNA libraries from which two overlapping clones (1100 and 2425 bp, respectively) were obtained

IL-33 expression is lower in current smokers at both transcriptomic and protein level

INTRODUCTION: IL-33 is a pro-inflammatory cytokine thought to play a role in the pathogenesis of asthma and COPD. A recent clinical trial using the anti-IL33 antibody showed a reduction in exacerbation and improved lung function in ex-smokers but not current smokers with COPD. In this study, we aimed to understand the effects of smoking status on IL-33. METHODS: We investigated the association of smoking status with the level of gene expression of IL33 in the airways in eight independent transcriptomic studies of lung airways. Additionally, we performed western blot and immunohistochemistry for IL-33 in lung tissue to assess protein levels. RESULTS: Across the bulk RNA-sequencing datasets, IL-33 gene expression and its signaling pathway were significantly lower in current- compared to ex- or never-smokers and increased upon smoking cessation (p<0.05). Single-cell sequencing showed that IL-33 is predominantly expressed in resting basal epithelial cells and decreases during the differentiation process triggered by smoke exposure. We also found a higher transitioning of this cellular sub-population into a more differentiated cell type during chronic smoking, potentially driving the reduction of IL-33. Protein analysis demonstrated lower IL-33 levels in lung tissue from COPD current- compared to ex-smokers and a lower proportion of IL-33 positive basal cells in current versus ex-smoking controls. CONCLUSION: We provide strong evidence that cigarette smoke leads to an overall reduction in IL33 expression in both transcriptomic and protein level and this may be due to the decrease in resting basal cells. Together, these findings may explain the clinical observation that a recent antibody-based anti-IL-33 treatment is more effective in ex- than current smokers with COPD